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Órgano Oficial del Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz

2003, Number 3

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Salud Mental 2003; 26 (3)

Trastornos bioquímicos y metabólicos de la bulimia nervosa y la alimentación compulsiva

Hernández-Escalante V, Trava-García M, Bastarrachea-Sosa R, Laviada-Molina H

Language: Spanish
References: 39
Page: 9-15
PDF size: 376.27 Kb.


ABSTRACT

Binge eating disorder (BED) patients are generally obese, whereas obesity is infrequent in bulimia nervosa (BN) patients, who tend to have a Body Mass Index (BMI) within normal ranges. Metabolic disorders are common in these patients. For example, BED patients tend towards obesity because their repeated efforts at weight-loss produce cyclical changes in weight, which can increase metabolic efficiency. As a result, an energy conservation state that promotes weight gain can be induced, leading to even greater efforts at weight-loss. Psychopathologies such as depression are also extremely frequent in both these patient types. Both the hypothalamus-hypophysis-adrenal (HHA) axis and serotonin alterations may be related to decreases in leptin, which may contribute to the genesis of eating binges in BN. Diurnal leptin secretion patterns are altered in patients with compulsive eating episodes, who experience cessation of normal leptin levels two hours after the mid-day meal. As is to be expected, obese BED patients have a higher frequency of elevated leptin levels, which is positively correlated to BMI. High levels of neuropeptide Y (NPY), a strong appetite potentiator, have been reported in normal-weight BN patients, independently of BMI. Low gastrin stimulating neuropeptide (GRP) levels have been found in BN patients, which act as a central level anorexigenic. Paradoxically, it is also common to find elevated levels of an appetite inhibitor, such as cholecystokonin-pancreomycine (CCK-PM), positively correlated to the increase in ingested portions. Elevated beta-endorphin serum levels have been reported, which suggest elevated opioid tone in BN patients. A possible decrease in dipeptilpeptidase IV (DPP IV) enzyme activity is still controversial. This decrease inactivates glucagon, which can have a determinant impact in satiety control and can even affect the immune system. Noradrenalin (NA) and serotonin (5-HT) serum levels are lower in BN patients in comparison to healthy individuals, whereas their dopamine levels are similar or lower than control subjects. These levels are strongly related to psychopathologies such as depression. Diminished basal tryptophan serum levels (the main precursor of serotonin) have been found in BN patients, but with no differences in the tryptophan/long-chain neutral amino acids (LNAA) ratio, even after glucose ingestion. Clinical trials have shown female BN patients to be more vulnerable to mood changes induced by a tryptophan-deficient diet, suggesting altered modulation of the serotonin central neuronal systems. An exaggerated insulin response has been reported in patients with relatively infrequent vomiting and binges, and stable weight. In contrast, no insulin response peaks occur in patients with more frequent vomiting and binges, unstable weight, and no basal eating pattern associated with high plasmatic cortisol levels. Insulin response is normal in patients that have not had binges or serious compensatory behavior over a four-week period. Bulimia nervosa patients do not experience the normal increase in cortisol levels one hour after eating, and abnormalities have been reported in the suppression test using dexametasone. A correlation between blood glucose levels and mood has been reported for BN patients, but not for control subjects. In addition, compulsive eating episodes have been induced in BN patients 10 to 60 minutes after glucose injection, whereas this caused no episodes in control subjects, and mainly lowered ingestion of sweets. Marked changes have been reported in the Hypothalamus-Hypophysis-Adrenal (HHA) axis, even in the absence of weight or BMI change, suggesting central activation of corticotrophin stimulating hormone (CRH) and/or synergic factors. This may also suggest alterations in signals between the intestine and the brain associated with BN and compulsive eating disorders in general. Menstrual disorders affecting normal-weight BN patients are accompanied by gonadotropin abnormalities comparable to low-weight anorexic patients in some patients. Polycystic ovary syndrome is common in women with BN. Amenorrheic women with BN also have low luteinizing hormone (LH) levels, altered gonadotropin freeing hypothalamus hormone (GnRH) and prolactin responses, and decreased 17-Β estradiol levels (E2). Testosterone levels are generally normal in BN patients, though there are morning increases in neuroactive peripheral steroids such as hydroprogesterone, dehydroepiandrosterone (DEA), and its sulphated metabolite (DHEAS). Additionally, the immune system is affected, and IGF-1 levels can decrease. Similarities between the serotoninergic, noradrenergic and dopaminergic system imbalances found in BN patients and those that occur during depression are currently controversial, though they may prove promising for preventive and therapeutic approaches to BN.


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